Uveitis is a diverse group of potentially sight-threatening intraocular inflammatory diseases that includes Behets disease, birdshot retinochoroidopathy, VogtKoyanagiHarada disease, sympathetic ophthalmia, and ocular sarcoidosis. The etiology of uveitis is not fully understood but may be linked to autoimmunity. Cytokine signaling plays critical roles in the pathology of uveitis. IL-17 is substantially elevated in freshly isolated PBMC from patients with active uveitis, as well as in PBMC and lymph nodes of mice with experimental autoimmune uveitis (EAU), a model of human uveitis. The increase in IL-17 upregulates TNF- in the retina, suggesting a mechanism by which Th17 cells contribute to ocular pathology during uveitis. Transcription factors that regulate Th17 development and effector functions also play important roles in pathophysiology of uveitis. Thus, identifying transcription factors that regulate cytokine signaling and Th17 cells has therapeutic potential in the treatment of uveitis. We previously reported that the increased secretion of IL-1 in the retina by neutrophils, macrophages, and dendritic cells during ocular inflammation and show that loss of IL-1R signaling confers protection from experimental autoimmune uveitis. Amelioration of experimental autoimmune uveitis in Il1r-deficient mice was associated with reduced infiltration of inflammatory cells into the retina and decreased numbers of uveitogenic Th17 cells that mediate uveitis. A collaborative study with Rachel Caspi's Lab at NEI revealed that STAT-3-independent production of IL-17 by mouse innate-like T cells can control ocular inflammatory responsesn. These and other findings indicate the possible manipulating levels of STAT3 and SOCS3 proteins for the treatment of ocular inflammatory diseases